Inclusion body hepatitis (IBH) is an economically important, emerging problem in broiler chickens in several geographical regions in Southeast Asia, Europe, Middle East, Europe, Australia, New Zealand, North America, Mexico, Central and South America (Gomis et al., 2006; Ojkic et al., 2008b). Historically, IBH has been identified as a secondary disease in broiler chickens associated with common immunosuppressive agents such as infectious bursal disease virus (IBDV) and chicken anemia virus (CAV) (Gomis et al., 2006). Pathogenesis of IBH is not clear due to multiple factors associated with its host, pathogen and the environment (Erny et al., 1991; Gomis et al., 2006; Grimes, 1992; 2007; Mendelson et al., 1995).
The disease is manifested as sudden onset of increased mortality of 1-10% (Gomis et al., 2006), and occasionally exceeding 30-40% (Barr and Scott, 1988; Erny et al., 1991), with a short clinical course of 4-5 days. Inclusion body hepatitis (IBH) is an acute viral disease of 2-7 week old broiler chickens (Adair and Fitzgerald, 2008). The affected chickens typically have pale, friable, swollen livers with focal to extensive necrosis, and large basophilic INIB in hepatocytes (Reece et al., 1986a). Since the initial studies, IBH has been reported in North America (Alvarado et al., 2007; El-Attrache and Villegas, 2001; Gomis et al., 2006; Ojkic et al., 2008b), Mexico (Antillon and Lucio, 1974; Sarfati, 1991), Europe (Hoffman et al., 1975; Young et al., 1972), Japan (Itakura et al., 1974b; Otsuki et al., 1976), New Zealand (Christensen and Saifuddin, 1989), Australia (Grimes, 1992; Reece et al., 1986a; Wells et al., 1977), and several Latin American countries (Toro et al., 1999). Control of IBH has been attempted in several countries by vaccination of boiler breeders and broilers with inactivated, autogenous vaccines (Alvarado et al., 2007; Cowen, 1992).
A fowl adenovirus serotype-5 (FAdV-5), Tipton strain was incriminated in the etiology of IBH (Bickford, 1972; Fadly and Winterfield, 1973; McFerran et al., 1976b; Rosenberger et al., 1974). Thereafter, all other serotypes of FAdV have been associated with outbreaks of IBH in chickens: FAdV-1 (Singh et al., 1996); FAdV-2 (Philippe et al., 2005); FAdV-3 and FAdV-4 (Grimes and King, 1977a); (McFerran et al., 1976b); FAdV-4 (Mazaheri et al., 1998); FAdV-6, FAdV-7, FAdV-8, FAdV-8a, FAdV-8b and FAdV-11 (Grimes et al., 1977b; Kefford and Borland, 1979; Ojkic et al., 2005; Ojkic et al., 2008a); FAdV-9 (Grimes et al., 1978b); FAdV-7 and FAdV-10 (Barr and Scott, 1988); FAdV-11 (Mendelson et al., 1995) and FAdV-12 (Saifuddin et al., 1992). The disease has been experimentally reproduced in broiler chickens with isolates from IBH outbreaks (Fadly and Winterfield, 1973; Wells and Harrigan, 1974).
Identification of IBH as a primary disease in broilers has urged the need of vaccines to control IBH at their parent level (Ahmad and Burgess, 2001; Grimes, 1992). Control of IBH has been attempted in several countries by vaccination of broiler breeders and broiler chickens with inactivated, autogenous, (Alvarado et al., 2007; Cowen, 1992) or chick-embryo propagated vaccines (Engormix, Mexico). In Australia, IBH is controlled by vaccination of broiler breeders with a commercial live, chick embryo liver cell grown vaccine containing a FAdV-8b strain (Intervet Australia, Pvt. Ltd.). Further, this vaccine was recommended to be administered by the eye-drop method in pullets (Grimes, 1992; 2007). The Australian Intervet FAdV vaccine is for the protection of chickens against homologous type-8 FAdV invection (IBH) up to 28 days of age, by vaccinating breeders.
Most cases of acute IBH are the result of vertical transmission of FAdV, and ensuring that breeder flocks have seroconverted prior to the onset of lay can prevent the disease (Grimes, 2007). Maternal antibodies have been shown to protect the progeny against the development of IBH, as shown by challenge of progeny of broiler breeders that had been vaccinated twice with an autogenous killed vaccine (comprising serotype FAdV-8, (8565 strain) and serotype FAdV-11, (1047 strain)] (Alvarado et al., 2007). Vaccination of broiler breeders with a live, (FAdV-8, (Esurient strain)) virulent strain during rearing also has been shown to protect progeny from IBH outbreaks (Grimes, 2007). Effective protection of progeny by dual vaccination of layer breeders against IBH and CAV has been shown to protect progeny against challenge with FAdV associated with IBH (Toro et al., 2001a).
Based on hexon gene loop 1 sequencing analysis, isolates from Canadian outbreaks of inclusion body hepatitis (IBH) have been found to be genetically related to FAdV-2 strain P7-A, FAdV-x11a, FAdV-8a strain TR-59, FAdV-8a/8b strain Ontario (equal percentage identity to FAdV-8a strain T8-A and FAdV-8b strain 764), and FAdV-11 strain 1047 (Ojkic et al., 2008b).
Since 2000, IBH has been responsible for severe economic losses in the Canadian broiler industry due to sudden onset of increased mortality lasting for 5-7 days (Gomis et al., 2006; Ojkic et al., 2008b). Although high mortality and economic losses have continued for several years in the Canadian broiler industry due to IBH, no commercial vaccines are available to-date in Canada, except limited application of autogenous vaccines (Ojkic et al., 2008a).